Research in the Colognato Lab focuses on investigating the
molecular mechanisms that control the development and function of
oligodendroglia. Oligodendroglia are specialized glial cells that are crucial
for neural networks in the brain and spinal cord to operate at maximum speed
and efficiency. The lab has been uncovering how developing oligodendroglia
interact with extracellular matrix proteins, both in their germinal niche as
they transition from neural stem cells to specialized glia, as well as in the
developing nerve tracts themselves, where final maturation and functional
integration takes place. Also, several projects study the reparative ability of
oligodendroglia in the adult brain, as the specialized myelin membranes that
oligodendroglia produce are damaged and/or dysfunctional in many
neurodegenerative conditions, including Multiple Sclerosis.

We study a specialized glial cell, the oligodendrocyte, which
myelinates axons in the brain and spinal cord. The laminin family of
adhesion proteins are good candidates to regulate oligodendrocytes and
the process of myelination: brain defects, including abnormal
myelination, occur in the absence of normal laminin signaling. Our work
has demonstrated that adhesive interactions with laminins can stimulate
oligodendrocytes to survive and differentiate, at least in part by
altering interactions with growth factors and downstream signal
transduction mechanisms. We are now learning how laminins and
laminin-regulated signaling molecules operate during normal brain
development and function, as well as during diseases where myelination
is dysregulated. An understanding of the mechanisms that control
myelination will be important for two areas of human health: (1) during
development, where normal myelination is crucial, and (2), during brain
and spinal cord repair, which is hampered by the inability of the
central nervous system (CNS) to regenerate. Remyelination failure leads
to the neurodegeneration in demyelinating diseases such as Multiple
Sclerosis, and is predicted to play a role in the neurodegeneration
process in diseases such as Alzheimer's, and, following CNS injury in
which new neuronal connections need to be myelinated to achieve
functional recovery. One of our long-term objectives is to design
pharmacological strategies to enhance myelination and myelin repair in
the damaged nervous system.

Colognato, H. and Tzvetanova, I.D. Glia unglued: How signals from the
extracellular matrix regulate the development of myelinating glia. Dev.
Neurobiology special issue entitled “The role of extracellular matrix in
nervous system development and maintenance.” In press.

The Colognato Lab studies the
development and function of glial cells, in particular oligodendroglia and
astrocytes, which are specialized neural cells found in the brain and spinal
cord. Several projects in the lab focus on the role of adhesion receptors and
extracellular matrix proteins as regulatory factors in the genesis,
development, and function of oligodendroglia, which are born in a specialized
stem cell niche in the developing perinatal brain. Additional projects focus on
the role of adult oligodendroglia in repair following damage to nerve tracts,
as well as on the role of astrocyte extracellular matrix proteins that
influence the development and function of the blood-brain barrier.

We study a
specialized glial cell, the oligodendrocyte, which myelinates axons in
the brain and spinal cord. The laminin family of adhesion proteins are
good candidates to regulate oligodendrocytes and the process of
myelination: brain defects, including abnormal myelination, occur in the
absence of normal laminin signaling. Our work has demonstrated that
adhesive interactions with laminins can stimulate oligodendrocytes to
survive and differentiate, at least in part by altering interactions
with growth factors and downstream signal transduction mechanisms. We
are now learning how laminins and laminin-regulated signaling molecules
operate during normal brain development and function, as well as during
diseases where myelination is dysregulated. An understanding of the
mechanisms that control myelination will be important for two areas of
human health: (1) during development, where normal myelination is
crucial, and (2), during brain and spinal cord repair, which is hampered
by the inability of the central nervous system (CNS) to regenerate.
Remyelination failure leads to the neurodegeneration in demyelinating
diseases such as Multiple Sclerosis, and is predicted to play a role in
the neurodegeneration process in diseases such as Alzheimer's, and,
following CNS injury in which new neuronal connections need to be
myelinated to achieve functional recovery. One of our long-term
objectives is to design pharmacological strategies to enhance
myelination and myelin repair in the damaged nervous system.